S100A9 polyclonal antibody
- Known as:
- S100A9 pab (anti-)
- Catalog number:
- PAB11470
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- S100A9 polyclonal antibody
Related genes to: S100A9 polyclonal antibody
- Gene:
- S100A9 NIH gene
- Name:
- S100 calcium binding protein A9
- Previous symbol:
- CAGB, CFAG
- Synonyms:
- P14, MIF, NIF, LIAG, MRP14, MAC387, 60B8AG, CGLB
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-19
- Date modifiied:
- 2018-05-02
Related products to: S100A9 polyclonal antibody
Related articles to: S100A9 polyclonal antibody
- Chronic rhinosinusitis with nasal polyps (CRSwNP) exhibits pronounced endotypic heterogeneity, with macrophages serving as key drivers of sustained mucosal inflammation. In this study, we identify S100A9 as a macrophage-derived alarmin that is markedly elevated in CRSwNP tissues. Integrative analyses of public bulk transcriptomic datasets and single-cell RNA-sequencing atlases demonstrated that S100A9 expression was predominantly enriched in macrophage clusters, where it showed strong co-expression with canonical M1-associated markers, while exhibiting limited expression in epithelial cell subsets. Spatial and correlation analyses further supported a close association between S100A9⁺ macrophages and epithelial barrier-related gene signatures. Functionally, shRNA-mediated silencing of S100A9 attenuated M1-like macrophage polarization, as evidenced by reduced expression of pro-inflammatory mediators and polarization markers, accompanied by a shift toward a less inflammatory macrophage phenotype. Conditioned media derived from S100A9-deficient macrophages significantly mitigated epithelial injury, leading to restoration of epithelial barrier integrity, as indicated by enhanced expression of tight junction proteins, including occludin and claudins. Importantly, S100A9 knockdown disrupted the pathogenic macrophage-epithelial inflammatory feedback loop, thereby dampening sustained inflammatory signaling and limiting epithelial barrier breakdown that perpetuates tissue damage in CRSwNP. Clinically, elevated S100A9 levels correlated with disease severity indices and effectively distinguished a macrophage-enriched inflammatory endotype of CRSwNP, highlighting S100A9 as both a mechanistic driver and a potential biomarker for disease stratification. Collectively, these findings position S100A9 as a mechanistic mediator and a promising therapeutic target for CRSwNP. - Source: PubMed
Publication date: 2026/05/06
Ji YunxiangLuan JiaYuan FangWang ZhaoWei RanSun Guangbin - Acinar-to-ductal metaplasia (ADM) is a pivotal step in pancreatic tumorigenesis, reversible in normal contexts but progressing to PanIN and pancreatic cancer (PC) in the presence of Kras mutation and inflammation. Thus, delineating exocrine cell heterogeneity and identifying regulators of ADM are essential for understanding pancreatic tumorigenesis. - Source: PubMed
Publication date: 2026/05/07
Yuan QihangChen JunhongLuo PengLiu KaiGuo FangyueXu YaoTong MengyingXiang HongShang Dong - Primary open-angle glaucoma (POAG) is a progressive optic neuropathy that leads to irreversible vision loss, primarily due to dysfunction of the trabecular meshwork (TM). Although impaired autophagy has been implicated in POAG pathogenesis, its molecular drivers remain poorly defined. This study systematically investigated autophagy-related genes (ATGs) in TM tissue from POAG patients. Transcriptomic datasets (GSE4316 and GSE27276) were analyzed to identify differentially expressed genes (DEGs). A curated list of autophagy-related genes (ATGs) from HADb and GeneCards was intersected with DEGs to identify differentially expressed ATGs (DEATGs). Functional analyses included Gene Ontology (GO) and KEGG pathway enrichment, protein-protein interaction (PPI) network construction, hub gene identification, immune cell infiltration profiling via single-sample gene set enrichment analysis (ssGSEA), and molecular docking to evaluate predicted interactions between latanoprost and hub proteins. A total of 990 DEGs were identified, including 15 DEATGs. Among these, S100A8 and S100A9 emerged as hub genes, exhibiting strong functional similarity and central roles within the PPI network. Enrichment analysis revealed significant involvement in autophagy regulation, tyrosine metabolism, and oxidative phosphorylation. Notably, molecular docking predicted high-affinity binding between latanoprost and S100A9. Immune profiling demonstrated significant alterations in both innate and adaptive immune cell populations, including a strong positive correlation between S100A9 expression and Th2 cell abundance. These findings suggest that S100A9 may act as a central regulator linking autophagy deficiency to immune dysregulation in POAG. Its predicted interaction with latanoprost highlights a potential molecular mechanism for pharmacologic modulation of TM homeostasis, supporting the therapeutic value of targeting S100A9-mediated autophagy-immune crosstalk in intraocular pressure control. - Source: PubMed
Publication date: 2026/03/11
Hu LiliPan ShaoxinChen GongLei MinAi MingLv XiangyunPan HaoningWang PengChang Rui - The most common ocular neoplasia among children is retinoblastoma. Currently, the diagnosis of this disease is essentially clinical, taking a biopsy is contraindicated owing to the high risk of causing metastasis. Therefore, it is imperative the development of a method to diagnose this disease through a non-invasive fashion. We choose tears as they fulfill the former precept. Through proteomic analysis we observed 52 up regulated and 48 down regulated proteins among retinoblastoma cases as compared to healthy children. Among these proteins, we identified several previously associated with retinoblastoma such as apolipoprotein A-1 (). We confirmed up regulation of and S100 binding calcium A9 () which revealed faithful concordance to the predicted values from mass spectrometry. - Source: PubMed
Publication date: 2026/04/22
Rodríguez-Rodríguez AndrésCalderón-González Karla GriselLuna-Arias Juan PedroMoctezuma-Dávila MarianaRangel-Charqueño MarthaYañez-Soto BernardoOlivares-Illana VanesaHernández-Monge Jesús - Immunotherapy has emerged as a promising strategy for multiple myeloma (MM), yet relapse remains frequent due to the immunosuppressive bone marrow (BM) microenvironment, characterized by T cell dysfunction and accumulation of immunosuppressive myeloid cells. The co-stimulatory receptor 4-1BB (CD137, TNFRSF9) can enhance T and NK cell effector functions, but its therapeutic utility in MM is not well established. Tasquinimod (TQ), a clinical-stage S100A9 inhibitor, offers a complementary approach by limiting the recruitment and activity of suppressive myeloid cells. - Source: PubMed
Publication date: 2026/05/04
Satilmis HaticeDenis AdrienVerheye EmmaVan der Vreken ArneZhan DewenCalliauw EvanTörngren MarieEriksson HelenaFaict SylviaDe Bruyne ElkeMenu ElineVanderkerken KarinDe Veirman Kim